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- Linnet, K.M., Dalsgaard, S., Obel, C., Wisborg, K., Henriksen, T.B., Rodriguez, Alina, Kotimaa, A., Moilanen, I., Thomsen, P.H., Olsen, J., Järvelin, M.R.
(författare)
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Maternal lifestyle factors in pregnancy and risk of Attention-Deficit Hyperactivity Disorders: A review of current evidence.
- 2003
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Ingår i: American Journal of Psychiatry. ; 160:6, s. 1028-1040
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Tidskriftsartikel (refereegranskat)
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- Nilsson, S, et al.
(författare)
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Mechanisms of estrogen action
- 2001
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Ingår i: Physiological reviews. - : American Physiological Society. - 0031-9333 .- 1522-1210. ; 81:4, s. 1535-1565
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Tidskriftsartikel (refereegranskat)abstract
- Our appreciation of the physiological functions of estrogens and the mechanisms through which estrogens bring about these functions has changed during the past decade. Just as transgenic mice were produced in which estrogen receptors had been inactivated and we thought that we were about to understand the role of estrogen receptors in physiology and pathology, it was found that there was not one but two distinct and functional estrogen receptors, now called ERα and ERβ. Transgenic mice in which each of the receptors or both the receptors are inactive have revealed a much broader role for estrogens in the body than was previously thought. This decade also saw the description of a male patient who had no functional ERα and whose continued bone growth clearly revealed an important function of estrogen in men. The importance of estrogen in both males and females was also demonstrated in the laboratory in transgenic mice in which the aromatase gene was inactivated. Finally, crystal structures of the estrogen receptors with agonists and antagonists have revealed much about how ligand binding influences receptor conformation and how this conformation influences interaction of the receptor with coactivators or corepressors and hence determines cellular response to ligands.
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- Suska, F., et al.
(författare)
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IL-1a, IL-1ß and TNF-a secretion during in vivo/ex vivo cellular interactions with titanium and copper
- 2003
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Ingår i: Biomaterials. - 0142-9612 .- 1878-5905. ; 24:3, s. 461-468
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Tidskriftsartikel (refereegranskat)abstract
- Titanium (Ti) and copper (Cu) were used to evaluate cytokine secretion around materials with different chemical properties. Ti disks were coated with Cu or left uncoated. The disks were inserted subcutaneously in rats for 1, 3, 12, 18, 24 and 48h. Interleukin-1a (IL-1a), IL-1ß and tumor necrosis factor-a (TNF-a) concentrations were measured in vivo around the materials, in sham operated sites, and after ex vivo incubation of surface adherent cells. Ti and Cu revealed distinct cytokine expression patterns. Cu recruited cells showed higher and prolonged release of IL-1a than Ti at longer times (>24h), whereas Ti exhibited a transient IL-1a response at earlier periods (<24h). An early enhanced secretion of TNF-a characterized Ti. Low amounts of IL-1ß were found around both materials. Sham site recruited cells produced lower levels of cytokines. The results after ex vivo incubations were similar to those in vivo. This study shows that material chemical properties influence early cytokine production. The Ti-associated transient rise of IL-1a and TNF-a may be of importance for the early tissue response around biocompatible materials, while a delayed high IL-1a expression could be a marker of inflammation induced by toxic materials. © 2002 Elsevier Science Ltd. All rights reserved.
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| 9. |
- Brunette, Donald M, et al.
(författare)
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Titanium in Medicine : material science, surface science, engineering, biological responses and medical applications
- 2001
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Bok (övrigt vetenskapligt/konstnärligt)abstract
- This comprehensive book provides state-of-the-art scientific and technical information in a clear format and consistent structure making it suitable for formal course work or self-instruction. The authors are drawn not only from academic institutions but also from industry, so that practical aspects of implant fabrication and material handling are covered that are often lacking in biomaterials texts. Besides readers with a general interest in biomaterials, the book will interest materials investigators, surgeons and dentists using titanium implants, medical scientists and engineers, as well as lecturers at universities or institutes who would benefit by having ready access to authoritative information on the use of titanium for implants, devices and instruments. More information: http://www.titaniuminmedicine.com.
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- Gromada, J, et al.
(författare)
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Nateglinide, but not repaglinide, stimulates growth hormone release in rat pituitary cells by inhibition of K+ channels and stimulation of cyclic AMP-dependent exocytosis
- 2002
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Ingår i: European Journal of Endocrinology. - : Oxford University Press (OUP). - 1479-683X .- 0804-4643. ; 147:1, s. 133-142
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Tidskriftsartikel (refereegranskat)abstract
- Objective: GH causes insulin resistance, impairs glycemic control and increases the risk of vascular diabetic complications. Sulphonylureas stimulate GH secretion and this study was undertaken to investigate the possible stimulatory effect of repaglinide and nateglinide, two novel oral glucose regulators, on critical steps of the stimulus-secretion coupling in single rat somatotrophs. Methods: Patch-clamp techniques were used to record whole-cell ATP-sensitive K+ (K-ATP) and delayed outward K+ currents, membrane potential and Ca2+-dependent exocytosis. GH release was measured from perifused rat somatotrophs. Results: Both nateglinide and repaglinide dose-dependently suppressed K-ATP channel activity with half-maximal inhibition being observed at 413 nM and 13 nM respectively. Both compounds induced action potential firing in the somatotrophs irrespective of whether GH-releasing hormone was present or not. The stimulation of electrical activity by nateglinide, but not repaglinide, was associated with an increased mean duration of the action potentials. The latter effect correlated with a reduction of the delayed outward K+ current, which accounts for action potential repolarization. The latter effect had a K-d of 19 muM but was limited to 38% inhibition. When applied at concentrations similar to those required to block K-ATP channels, nateglinide in addition potentiated Ca2+-evoked exocytosis 3.3-fold (K-d = 3 muM) and stimulated GH release 4.5-fold. The latter effect was not shared by repaglinide. The stimulation of exocytosis by nateglinide was mimicked by cAMP and antagonized by the protein kinase A inhibitor Rp-cAMPS. Conclusion: Nateglinide stimulates GH release by inhibition of plasma membrane K+ channels, elevation of cytoplasmic cAMP levels and stimulation of Ca2+-dependent exocytosis. By contrast, the effect of repaglinide was confined to inhibition of the K-ATP channels.
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